HPRG Double Nickase Plasmid (h): sc-404772-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HPRG Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- HPRG Double Nickase Plasmid (h) and HPRG Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HRG. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HPRG Double Nickase Plasmid (h) | sc-404772-NIC | 20 µg | $410.00 | |||
HPRG Double Nickase Plasmid (h2) | sc-404772-NIC-2 | 20 µg | $410.00 |
HRG encodes histidine-rich glycoprotein (HPRG), a secreted plasma protein that binds heparan sulfate, plasminogen, fibrinogen, and divalent metals to modulate coagulation and fibrinolysis. HPRG participates in extracellular matrix interactions and platelet–endothelial processes, linking vascular homeostasis with innate immune regulation through effects on leukocyte adhesion and complement-related functions. By shaping pericellular proteolysis and cell–matrix signaling, HPRG influences angiogenic balance and inflammatory trafficking in diverse tissues. Altered HRG/HPRG abundance or activity has been associated with dysregulated thrombosis–inflammation crosstalk and tumor microenvironment biology, making it a relevant target for mechanistic studies.
HPRG Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HRG locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HRG. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt HRG function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of HRG-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.